The C. elegans hunchback homolog, hbl-1, controls temporal patterning and is a probable MicroRNA target

Shin Yi Lin; Steven M. Johnson; Mary Abraham; Monica C. Vella; Amy Pasquinelli; Chiara Gamberi; Ellen Gottlieb; Frank J. Slack

doi:10.1016/S1534-5807(03)00124-2

The C. elegans hunchback homolog, hbl-1, controls temporal patterning and is a probable MicroRNA target

Shin Yi Lin, Steven M. Johnson, Mary Abraham, Monica C. Vella, Amy Pasquinelli, Chiara Gamberi, Ellen Gottlieb, Frank J. Slack

Molecular Biology

Research output: Contribution to journal › Article › peer-review

289 Scopus citations

Abstract

Hunchback regulates the temporal identity of neuroblasts in Drosophila. Here we show that hbl-1, the C. elegans hunchback ortholog, also controls temporal patterning. Furthermore, hbl-1 is a probable target of microRNA regulation through its 3′UTR. hbl-1 loss-of-function causes the precocious expression of adult seam cell fates. This phenotype is similar to loss-of-function of lin-41, a known target of the let-7 microRNA. Like lin-41 mutations, hbl-1 loss-of-function partially suppresses a let-7 mutation. The hbl-1 3′UTR is both necessary and sufficient to downregulate a reporter gene during development, and the let-7 and lin-4 microRNAs are both required for HBL-1/GFP downregulation. Multiple elements in the hbl-1 3′UTR show complementarity to regulatory microRNAs, suggesting that microRNAs directly control hbl-1. MicroRNAs may likewise function to regulate Drosophila hunchback during temporal patterning of the nervous system.

Original language	English (US)
Pages (from-to)	639-650
Number of pages	12
Journal	Developmental cell
Volume	4
Issue number	5
DOIs	https://doi.org/10.1016/S1534-5807(03)00124-2
State	Published - May 1 2003

All Science Journal Classification (ASJC) codes

General Biochemistry, Genetics and Molecular Biology
Molecular Biology
Cell Biology
Developmental Biology

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10.1016/S1534-5807(03)00124-2

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@article{1c77e889bb694dac8e11cdf6777d2ef4,

title = "The C. elegans hunchback homolog, hbl-1, controls temporal patterning and is a probable MicroRNA target",

abstract = "Hunchback regulates the temporal identity of neuroblasts in Drosophila. Here we show that hbl-1, the C. elegans hunchback ortholog, also controls temporal patterning. Furthermore, hbl-1 is a probable target of microRNA regulation through its 3′UTR. hbl-1 loss-of-function causes the precocious expression of adult seam cell fates. This phenotype is similar to loss-of-function of lin-41, a known target of the let-7 microRNA. Like lin-41 mutations, hbl-1 loss-of-function partially suppresses a let-7 mutation. The hbl-1 3′UTR is both necessary and sufficient to downregulate a reporter gene during development, and the let-7 and lin-4 microRNAs are both required for HBL-1/GFP downregulation. Multiple elements in the hbl-1 3′UTR show complementarity to regulatory microRNAs, suggesting that microRNAs directly control hbl-1. MicroRNAs may likewise function to regulate Drosophila hunchback during temporal patterning of the nervous system.",

author = "Lin, {Shin Yi} and Johnson, {Steven M.} and Mary Abraham and Vella, {Monica C.} and Amy Pasquinelli and Chiara Gamberi and Ellen Gottlieb and Slack, {Frank J.}",

note = "Funding Information: We thank J. Abrahante and A. Rougvie for sharing unpublished data. We thank Y. Kohara and D. Fay for hbl-1 cDNAs, D. Fay for the integrated hbl-1::gfp fusion animals, R. Barstead for cDNA libraries, J. Ahringer for an hbl-1 RNAi plasmid in HT115(DE3), the C. elegans and C. briggsae genome sequencing consortia for sequence data, the CGC for providing strains, J. Simske for wIs79, O. Hobert for helpful discussions, and members of the Slack laboratory for critical reading of this manuscript. We thank G. Ruvkun for support during the initial stages of this work. This work was supported by NIH RO1 grant (GM50800) to E.G. and NIH R01 grant (GM62594) to F.J.S.",

year = "2003",

month = may,

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doi = "10.1016/S1534-5807(03)00124-2",

language = "English (US)",

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T1 - The C. elegans hunchback homolog, hbl-1, controls temporal patterning and is a probable MicroRNA target

AU - Lin, Shin Yi

AU - Johnson, Steven M.

AU - Abraham, Mary

AU - Vella, Monica C.

AU - Pasquinelli, Amy

AU - Gamberi, Chiara

AU - Gottlieb, Ellen

AU - Slack, Frank J.

N1 - Funding Information: We thank J. Abrahante and A. Rougvie for sharing unpublished data. We thank Y. Kohara and D. Fay for hbl-1 cDNAs, D. Fay for the integrated hbl-1::gfp fusion animals, R. Barstead for cDNA libraries, J. Ahringer for an hbl-1 RNAi plasmid in HT115(DE3), the C. elegans and C. briggsae genome sequencing consortia for sequence data, the CGC for providing strains, J. Simske for wIs79, O. Hobert for helpful discussions, and members of the Slack laboratory for critical reading of this manuscript. We thank G. Ruvkun for support during the initial stages of this work. This work was supported by NIH RO1 grant (GM50800) to E.G. and NIH R01 grant (GM62594) to F.J.S.

PY - 2003/5/1

Y1 - 2003/5/1

N2 - Hunchback regulates the temporal identity of neuroblasts in Drosophila. Here we show that hbl-1, the C. elegans hunchback ortholog, also controls temporal patterning. Furthermore, hbl-1 is a probable target of microRNA regulation through its 3′UTR. hbl-1 loss-of-function causes the precocious expression of adult seam cell fates. This phenotype is similar to loss-of-function of lin-41, a known target of the let-7 microRNA. Like lin-41 mutations, hbl-1 loss-of-function partially suppresses a let-7 mutation. The hbl-1 3′UTR is both necessary and sufficient to downregulate a reporter gene during development, and the let-7 and lin-4 microRNAs are both required for HBL-1/GFP downregulation. Multiple elements in the hbl-1 3′UTR show complementarity to regulatory microRNAs, suggesting that microRNAs directly control hbl-1. MicroRNAs may likewise function to regulate Drosophila hunchback during temporal patterning of the nervous system.

AB - Hunchback regulates the temporal identity of neuroblasts in Drosophila. Here we show that hbl-1, the C. elegans hunchback ortholog, also controls temporal patterning. Furthermore, hbl-1 is a probable target of microRNA regulation through its 3′UTR. hbl-1 loss-of-function causes the precocious expression of adult seam cell fates. This phenotype is similar to loss-of-function of lin-41, a known target of the let-7 microRNA. Like lin-41 mutations, hbl-1 loss-of-function partially suppresses a let-7 mutation. The hbl-1 3′UTR is both necessary and sufficient to downregulate a reporter gene during development, and the let-7 and lin-4 microRNAs are both required for HBL-1/GFP downregulation. Multiple elements in the hbl-1 3′UTR show complementarity to regulatory microRNAs, suggesting that microRNAs directly control hbl-1. MicroRNAs may likewise function to regulate Drosophila hunchback during temporal patterning of the nervous system.

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ER -

The C. elegans hunchback homolog, hbl-1, controls temporal patterning and is a probable MicroRNA target

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